Holehouse E L, Liu M L, Aponte G W
Department of Nutritional Sciences, University of California, 119 Morgan Hall, Berkeley, CA 94720, USA.
Biochim Biophys Acta. 1998 Feb 5;1390(1):52-64. doi: 10.1016/s0005-2760(97)00176-8.
Intestinal-fatty acid binding protein (I-FABP) has been proposed to target long chain fatty acids (LCFA) to triglyceride synthesis pathways in the intestinal epithelium. In the present studies hBRIE 380i cells, which endogenously express I-FABP only when fully differentiated, were used to investigate the role of I-FABP in LCFA incorporation and targeting by examining the relative distribution of [3H]-oleic acid in cellular lipids in these cells. [3H]-oleic acid incorporation into triglyceride was significantly higher in hBRIE 380i cells expressing I-FABP than in cells not expressing I-FABP. After 15 min, 1 and 4 h of incubation, cells expressing I-FABP incorporated 24.0%, 34.0% and 43.9% of [3H]-oleic acid into triglyceride, while newly confluent cells (no I-FABP expression) incorporated 15.6%, 18.3% and 31.9%. An I-FABP negative cell line, hBRIE 380i-neg cells, was stably transfected to investigate the effect of adding I-FABP to small intestinal epithelial cell lines. No measurable differences in [3H]-oleic acid incorporation into triglyceride was detected in these transfectants. Additionally I-FABP expression had no effect on [3H]-oleic acid incorporation or distribution within phospholipid subclasses in hBRIE 380i or transfected hBRIE 380i-neg fabpi cells. Our data from hBRIE 380i cells suggest that I-FABP can target LCFA to triglyceride synthesis pathway. However, endogenous I-FABP expression was also correlated to cellular differentiation and therefore raises the possibility that other differentiation-dependent factors may have a role in LCFA targeting. Because no effects of I-FABP were detected in the transfected hBRIE 380i-neg fabpi cells, it is concluded that factors in addition to I-FABP play a major role in determining the metabolic fate of LCFA in small intestinal epithelial cells. (c) 1998 Elsevier Science B.V.
肠脂肪酸结合蛋白(I-FABP)被认为可将长链脂肪酸(LCFA)导向肠上皮细胞中的甘油三酯合成途径。在本研究中,hBRIE 380i细胞仅在完全分化时才内源性表达I-FABP,通过检测这些细胞中[3H] -油酸在细胞脂质中的相对分布,来研究I-FABP在LCFA掺入和导向中的作用。表达I-FABP的hBRIE 380i细胞中,[3H] -油酸掺入甘油三酯的量显著高于不表达I-FABP的细胞。在孵育15分钟、1小时和4小时后,表达I-FABP的细胞分别将24.0%、34.0%和43.9%的[3H] -油酸掺入甘油三酯,而新汇合的细胞(不表达I-FABP)分别掺入15.6%、18.3%和31.9%。构建了一个I-FABP阴性细胞系hBRIE 380i-neg细胞,并对其进行稳定转染,以研究向小肠上皮细胞系中添加I-FABP的效果。在这些转染细胞中,未检测到[3H] -油酸掺入甘油三酯有可测量的差异。此外,I-FABP的表达对hBRIE 380i或转染的hBRIE 380i-neg fabpi细胞中[3H] -油酸掺入或在磷脂亚类中的分布没有影响。我们从hBRIE 380i细胞获得的数据表明,I-FABP可将LCFA导向甘油三酯合成途径。然而内源性I-FABP的表达也与细胞分化相关,因此增加了其他分化依赖性因子可能在LCFA导向中起作用的可能性。由于在转染的hBRIE 380i-neg fabpi细胞中未检测到I-FABP的作用,得出的结论是,除I-FABP外的其他因子在决定小肠上皮细胞中LCFA的代谢命运方面起主要作用。(c)1998爱思唯尔科学出版社B.V.